It is well established that both acne and male-pattern baldness are the result of accumulation of androgens, particularly testosterone and dihydrotestosterone.
Acne begins at puberty when the increase in circulating androgens causes an increase in size and activity of the pilosebaceous glands.
Male-pattern baldness is common and it is well-recognized to be familial and proven to require the presence of androgens. (Merck Manual 15th Ed.pg. 2277 and 2281) It is recognized that circulating testosterone is metabolized in the skin to dihydrotestosterone (DHT) (Benson et al U.S. Pat. No. 4,088,760) which is 4 to 20 times as potent an androgen as testosterone.
It is postulated that the varying rates of formation and high accumulations of DHT in the skin give rise to the pathogenesis of acne and other androgen-related conditions, particularly male-pattern baldness.
Male-pattern baldness, wherein hair follicles, primarily on the crown of the head, shrink in size, producing an ever thinner and thinner hair until ultimately many follicles shrink to a point where they no longer can produce a hair, i.e., they become dormant. Individuals showing male-pattern baldness begin to lose their hair early in life, often in their twenties. It is well documented that male-pattern baldness is a type of sex-influenced inheritance, with the allele for pattern baldness being dominant in males and recessive in females. The precise mechanism of androgen conversion and toxic accumulation is not thoroughly understood.
Over the past several years, extracellular androgen-binding macro molecules have been identified that are distinct from the intracellular androgen-receptors. The best characterized are the testosterone-extradiol binding globulin (TeBG) from serum and the androgen binding protein (ABP) from the testes, as disclosed in "Extracellular Androgen Binding Proteins" by Bardin et al in Ann.Rev. Physiol, 1981, pages 189-198. A variety of in vivo studies have suggested that TeGB-bound testosterone is less available for expression of biological activity than is the free steroid.
Although the absence of localized accumulation of androgens is believed fundamentally necessary to counter acne and expression of baldness in males, other factors are also important.
Basically, there are different methods by which such biochemical activities are controlled. One, as mentioned, is genetic regulation and accumulation and enzymatic regulation as well. Most often these regulatory mechanisms function as feedback control systems that continually monitor a cell's biochemistry and make corrections as needed. But, on occasion, substances from without also control intracellular biochemical reactions, by inhibiting or activating one or more of the intracellular control systems.
One such controlling extrinsic factor is the topical application of ionizable salts to disassociate the testosterone or DHT. Such ionizable salts effect changes in the hormones or protein-associated hormones. Such effects include interrupting the hormone-protein linkages as well as breaking the complex structures to inactivate the active androgenic components of these molecules. Removal or inactivation of the active androgenic elements removes the toxic effects of the androgens, testosterone and/or DHT, the congestion at the hair follicles leading to clinical acne and/or male pattern baldness.
A number of researchers have postulated that phospholipid metabolism may be a factor in cellular proliferation and follicular metabolism (Yu and Tsai et al of Roche Institute) Cell Vol 52 p.63-71 1988 and Science V 243 p 522-25; V 250 p.982-84. The phospholipids activate guanosine triphosphatase (GTPase) which decomposes or otherwise inactivates testosterone and/or DHT. Suitable phospholipids, for example, include complexes of lecithins, complexed with saturated and unsaturated fatty acids or oils containing some inositol and nitrogenous bases such as choline and choline chloride. Phosphoric acid in small amounts insures the stability of such complexes when topically applied.